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Updated: Dec 28, 2025
Characterization of Molecular Mechanisms of In vivo UVR Induced Cataract
Published on: November 28, 2012
UVR-B-induced NKR-1 Expression in Ocular Tissues is blocked by Substance P Receptor Antagonist Fosaprepitant in the
Janine Gross1, Alfred R Wegener1, Martin Kronschläger2
1Department of Ophthalmology, University of Bonn, Bonn, Germany.
Abstract:
Purpose: To investigate the effect of NKR-1 antagonists in an established UVR-B-induced cataract mouse model. Furthermore, to examine the expression of pro-inflammatory cytokines/chemokines in mouse eyes following unilateral UVR-B exposure.Methods: Mice received intraperitoneally injections of Fosaprepitant and Spantide I, before and after unilateral exposure to UVR-B. After day 3 and 7 post-exposure, ocular tissues were extracted for the detection of NKR-1 protein level by ELISA.Results: Pretreatment with Fosaprepitant decreases NKR-1 expression in exposed ocular tissues as well as in the unexposed lens epithelium compared to the saline group. Spantide I treatment showed a tendency of NKR-1 overexpression in ocular tissues.Conclusion: The clinically approved NKR-1 receptor antagonist Fosaprepitant decreases NKR-1 protein expression effectively not only in the exposed but also in the unexposed partner eye in a UVR-B irradiation mouse model. No effect was seen on the protein concentration of pro-inflammatory cytokines/chemokines in either eye.
Insights
The neurokinin-1 receptor (NKR-1) antagonist Fosaprepitant reduced NKR-1 expression in a UVR-B-induced cataract mouse model. This effect was observed in both exposed and unexposed eyes, with no impact on inflammatory markers.
Area of Science:
- Ophthalmology
- Pharmacology
- Molecular Biology
Background:
- Ultraviolet B (UVR-B) radiation is a known cause of cataracts.
- Neurokinin-1 receptor (NKR-1) antagonists are being investigated for various therapeutic applications.
- The role of NKR-1 in UVR-B-induced ocular damage remains unclear.
Purpose of the Study:
- To evaluate the efficacy of NKR-1 antagonists in a UVR-B-induced cataract mouse model.
- To assess the impact of NKR-1 antagonism on pro-inflammatory cytokine and chemokine expression in the eye following UVR-B exposure.
Main Methods:
- Mice were treated with Fosaprepitant or Spantide I before and after unilateral UVR-B exposure.
- Ocular tissues were collected on days 3 and 7 post-exposure.
- NKR-1 protein levels were quantified using ELISA.
Main Results:
- Fosaprepitant pretreatment significantly decreased NKR-1 expression in both exposed and unexposed ocular tissues.
- Spantide I treatment showed a trend towards increased NKR-1 expression.
- No significant changes in pro-inflammatory cytokine/chemokine concentrations were observed in either eye.
Conclusions:
- The NKR-1 antagonist Fosaprepitant effectively reduces NKR-1 protein expression in a UVR-B-induced cataract mouse model.
- This reduction occurs in both the directly exposed and the contralateral unexposed eye.
- NKR-1 antagonism did not influence the levels of key pro-inflammatory mediators in this model.
